<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Montico B</submitter><funding>Associazione Italiana per la Ricerca sul Cancro</funding><funding>Ministero della Salute</funding><pagination>53</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11827140</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>44(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>About 50% of cutaneous melanoma (CM) harbors the activating BRAF&lt;sup>V600&lt;/sup> mutation which exerts most of the oncogenic effects through the MAPK signaling pathway. In the last years, a number of MAPK modulators have been identified, including Spry1. In this context, we have recently demonstrated that knockout of Spry1 (Spry1&lt;sup>KO&lt;/sup>) in BRAF&lt;sup>V600&lt;/sup>-mutant CM led to cell cycle arrest and apoptosis, repressed cell proliferation in vitro, and reduced tumor growth in vivo. Despite these findings, however, the precise molecular mechanism linking Spry1 to BRAF&lt;sup>V600&lt;/sup>-mutant CM remains to be elucidated.&lt;h4>Materials and methods&lt;/h4>Immunoprecipitation coupled to mass spectrometry was employed to gain insight into Spry1 interactome. Spry1 gene was knocke</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>Suppression of Spry1 reduces HIF1α-dependent glycolysis and impairs angiogenesis in BRAF-mutant cutaneous melanoma.</pubmed_title><pmcid>PMC11827140</pmcid><funding_grant_id>IG-23068</funding_grant_id><funding_grant_id>GR-2018-12366312</funding_grant_id><funding_grant_id>RF-2018-12365425</funding_grant_id><funding_grant_id>IG-23643</funding_grant_id><pubmed_authors>Giurato G</pubmed_authors><pubmed_authors>Covre A</pubmed_authors><pubmed_authors>Sigalotti L</pubmed_authors><pubmed_authors>Montico B</pubmed_authors><pubmed_authors>Lamberti J</pubmed_authors><pubmed_authors>Comelli M</pubmed_authors><pubmed_authors>Nassa G</pubmed_authors><pubmed_authors>Memoli D</pubmed_authors><pubmed_authors>Fratta E</pubmed_authors><pubmed_authors>Guerrieri R</pubmed_authors><pubmed_authors>Nyman TA</pubmed_authors><pubmed_authors>Maio M</pubmed_authors><pubmed_authors>Andreuzzi E</pubmed_authors><pubmed_authors>Colizzi F</pubmed_authors><pubmed_authors>Fejza A</pubmed_authors><pubmed_authors>Baboci L</pubmed_authors><pubmed_authors>Dal Bo M</pubmed_authors><pubmed_authors>Salvati A</pubmed_authors><pubmed_authors>Mongiat M</pubmed_authors><pubmed_authors>Sabatelli P</pubmed_authors><pubmed_authors>Steffan A</pubmed_authors><pubmed_authors>Weisz A</pubmed_authors><pubmed_authors>Bellazzo A</pubmed_authors><pubmed_authors>Camicia L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Suppression of Spry1 reduces HIF1α-dependent glycolysis and impairs angiogenesis in BRAF-mutant cutaneous melanoma.</name><description>&lt;h4>Background&lt;/h4>About 50% of cutaneous melanoma (CM) harbors the activating BRAF&lt;sup>V600&lt;/sup> mutation which exerts most of the oncogenic effects through the MAPK signaling pathway. In the last years, a number of MAPK modulators have been identified, including Spry1. In this context, we have recently demonstrated that knockout of Spry1 (Spry1&lt;sup>KO&lt;/sup>) in BRAF&lt;sup>V600&lt;/sup>-mutant CM led to cell cycle arrest and apoptosis, repressed cell proliferation in vitro, and reduced tumor growth in vivo. Despite these findings, however, the precise molecular mechanism linking Spry1 to BRAF&lt;sup>V600&lt;/sup>-mutant CM remains to be elucidated.&lt;h4>Materials and methods&lt;/h4>Immunoprecipitation coupled to mass spectrometry was employed to gain insight into Spry1 interactome. Spry1 gene was knocke</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Feb</publication><modification>2025-04-18T13:03:36.671Z</modification><creation>2025-04-04T02:26:14.407Z</creation></dates><accession>S-EPMC11827140</accession><cross_references><pubmed>39953610</pubmed><doi>10.1186/s13046-025-03289-8</doi></cross_references></HashMap>